Elsevier

Neuroscience Letters

Volume 208, Issue 1, 12 April 1996, Pages 41-44
Neuroscience Letters

Memantine reduces functional and morphological consequences induced by global ischemia in rats

https://doi.org/10.1016/0304-3940(96)12545-3Get rights and content

Abstract

In this study the effect of memantine, an antagonist at the N-methyl-d-aspartate receptor, on spatial learning deficit and on neuronal damage following transient: cerebral ischemia was evaluated. Global ischemia was induced by four-vessel-occlusion (4VO) for 20 min in rats. Memantine was administered 20 min before induction of ischemia at a dose of 10 or 20 mg/kg. One week after surgery spatial learning was tested in the Morris water maze. Treatment with the higher dose of memantine reduced the increase in escape latency and in swim distance induced by 4VO. Neuronal damage in the CA1 sector of the hippocampus and in the striatum produced by 4VO was significantly attenuated by 20 mg/kg memantine. Treatment with the lower dose of memantine bad no influence on the deficit in spatial learning and the neuronal damage resulting from ischemia. The present data demonstrate that treatment with a neuroprotective agent like memantine can reduce functional as well as morphological sequelae induced by ischemia.

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    Memantine (3,5-dimethyl-1-adamantanamine), a blood-brain barrier–permeable and selective NR2B antagonist, has been used clinically for the treatment of dementia and Parkinson disease for years. It also has neuroprotective effects in different neural injury models such as ischemia and hemorrhage.11-15 According to Walker,16 TBI and Alzheimer disease have similar pathophysiologic pathways, one of which is caused by increased concentrations of glutamate.

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Present address: Department of Neurology, Pauwelsstrasse 30, D52057 Aachen, Germany.

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